注射用丹参多酚酸治疗急性大动脉粥样硬化型脑梗死的疗效

目的 评价注射用丹参多酚酸对急性大动脉粥样硬化型脑梗死患者的临床疗效及安全性。方法 收集2016年9月-2017年8月山西医科大学第一医院收治的急性脑梗死患者100例,随机分为对照组及观察组,各50例。对照组予常规治疗,观察组在对照组基础上加用注射用丹参多酚酸,每次0.13 g加入250 mL 0.9%氯化钠中静滴,1次/d,治疗周期均为14 d。比较两组患者治疗前和治疗后神经功能缺损（NIHSS）评分、Barthel指数（BI）评分、血纤维蛋白原（FIB）、肝肾功能、心肌酶的变化以及不良反应。结果 治疗后,两组的NIHSS评分和BI评分均有显著改善（P<0.05）,且观察组NIHSS评分低于对照组（P<0.05）,BI评分高于对照组（P<0.05）;观察组血FIB与治疗前比较具有统计学差异（P<0.05）。两组患者用药前后肝肾功能、心肌酶未见明显变化,用药过程中无不良事件发生。结论 注射用丹参多酚酸可以改善急性大动脉粥样硬化型脑梗死患者的NIHSS评分和BI评分,并能在一定程度上降低血FIB水平;对患者的肝功能、肾功能、心肌酶等无明显影响,副作用小。     

注射用丹参多酚酸治疗急性期缺血性脑卒中的临床疗效及对血清细胞间黏附分子-1、肿瘤坏死因子-α水平的影响

目的 观察注射用丹参多酚酸对急性期缺血性脑卒中患者的临床疗效及安全性。方法 选取2018年6月—2019年6月保定市第一中心医院收治的100例急性期缺血性脑卒中住院患者,随机分为常规药物治疗组（对照组）和注射用丹参多酚酸治疗组（试验组）,各50例。对照组给予常规治疗,试验组在对照组基础上加用注射用丹参多酚酸0.13 g溶于250 mL0.9%氯化钠注射液中,静脉滴注、每天1次,两组均连续治疗2周。观察两组临床疗效,分别检测治疗前和治疗2周后两组患者血清细胞间黏附分子-1（ICAM-1）及肿瘤坏死因子-α（TNF-α）水平,并对患者进行美国国立卫生研究院卒中量表（NIHSS）评分及日常生活能力评定量表（BI）评分。结果 两组治疗前NIHSS评分、BI评分及血清ICAM-1、TNF-α水平无明显差异;治疗后两组NIHSS评分及血清ICAM-1、TNF-α水平均较同组治疗前降低,且试验组显著低于对照组（P＜0.05）,两组BI评分均较治疗前升高,且试验组BI评分较对照组显著升高（P＜0.05）;治疗后,对照组总有效率66.0%,试验组总有效率88.0%,两组比较差异显著（P＜0.05）。两组均未出现不良反应。结论 注射用丹参多酚酸可改善急性期缺血性脑卒中患者神经功能,可有效降低患者血清ICAM-1及TNF-α水平。     

注射用丹参多酚酸治疗恢复期脑干梗死的临床观察

目的 观察注射用丹参多酚酸治疗恢复期脑干梗死的疗效与安全性。方法 收集驻马店市中心医院2017年1月-2019年12月收治的恢复期脑干梗死住院患者80例,随机分为对照组及观察组,每组40例。对照组给予抗血小板聚集、降脂等治疗,观察组在对照组基础上加用注射用丹参多酚酸0.13 g+0.9%氯化钠注射液250 mL,静脉滴注,1次/d,两组均治疗14 d。比较两组患者美国国立卫生研究院卒中量表（NIHSS）评分、日常生活能力（Bathel指数）评分、疗效及不良反应。结果 治疗前两组患者的NIHSS评分、日常生活能力评分无统计学差异。治疗后,两组NIHSS评分均低于治疗前（P<0.05）,且观察组低于对照组（P<0.05）;两组日常生活能力评分均较治疗前提高（P<0.05）,且观察组较对照组明显提高（P<0.05）;观察组总有效率95.00%,明显高于对照组的82.50%（P<0.05）。两组未见明显的不良反应。结论 注射用丹参多酚酸治疗恢复期脑干梗死效果良好,可提高总有效率,且用药安全。     

注射用丹参多酚酸对脑梗死患者的临床疗效观察

目的 分析注射用丹参多酚酸对脑梗死患者的临床疗效。方法 选取黑龙江省第二医院40例脑梗死患者,随机分为观察组和对照组,对照组给予常规治疗,观察组在对照组治疗基础上加用注射用丹参多酚酸100 mg,1次/d静滴,疗程14d。比较两组患者神经功能改善情况及两组患者治疗有效率。结果 观察组及对照组治疗前NIHSS评分比较无明显差异;治疗后,观察组及对照组NIHSS评分均低于治疗前,同组治疗前后比较差异有统计学意义（P<0.05）;治疗后观察组NIHSS评分低于对照组,两者比较有显著差异（P<0.05）。观察组治疗总有效率高于对照组,差异具有统计学意义（P<0.05）。结论 脑梗死患者早期应用丹参多酚酸可有效改善神经功能,具有良好疗效。     

注射用丹参多酚酸治疗急性期脑梗死的临床观察

目的 观察注射用丹参多酚酸治疗急性期脑梗死的临床疗效及安全性。方法 124例急性期脑梗患者随机分为观察组、对照组,各62例。对照组给予抗血小板聚集、调控血脂、改善循环、营养神经、控制血压血糖及对症支持治疗脑梗死的药物治疗,必要时应用脱水剂;观察组在对照组治疗基础上加用注射用丹参多酚酸0.13 g溶于0.9%的氯化钠溶液250 mL缓慢静脉滴入,1次/d,共14 d。比较两组治疗前后美国国立卫生研究院卒中量表（NIHSS）评分、日常生活能力量表（Barthel Index,BI）评分改善的情况,患者治疗前后分别进行肝、肾功能化验,评价其安全性。结果 观察组与对照组治疗前NIHSS评分及BI评分比较差异没有统计学意义;治疗后,两组患者NIHSS评分显著降低,BI评分显著升高,治疗前后差异均具有统计学意义（P<0.05）;治疗后,与对照组比较,观察组患者BI评分显著升高,NIHSS评分显著降低,差异具有统计学意义（P<0.05）。治疗后,观察组患者的总有效率是79.03%,显著高于对照组的45.16%,差异具有统计学意义（P<0.05）。两组患者在用药期间未出现严重不良反应。结论 注射用丹参多酚酸可明显改善急性脑梗死患者的神经功能,提高患者的生活质量,是治疗急性脑梗死安全有效的方法。     

注射用丹参多酚酸联合阿司匹林治疗急性大动脉粥样硬化型脑梗死的临床研究

目的 观察注射用丹参多酚酸联合阿司匹林治疗急性大动脉粥样硬化型脑梗死临床疗效。方法 选取2017年2月-2018年1月在保定市第一中心医院就诊的急性大动脉粥样硬化型脑梗死患者202例作为研究对象,采用随机数字表法将患者分为对照组和观察组,每组各101例。对照组晨起空腹口服阿司匹林肠溶片,100 mg/次,1次/d。观察组在对照组治疗的基础上静脉输注注射用丹参多酚酸,0.13 g加入到生理盐水250 mL中稀释,1次/d。两组均治疗14 d。观察两组患者的临床疗效,同时比较两组治疗前后的美国国立卫生研究院卒中量表（NIHSS）评分、半乳糖凝集素-3（GLA-3）和白细胞介素-6（IL-6）水平。结果 治疗后,对照组和观察组的总有效率分别为63.4%和75.2%,两组总有效率比较差异具有统计学意义（P<0.05）。治疗后,两组组NIHSS评分均显著下降（P<0.05）,且观察组NIHSS评分显著低于对照组（P<0.05）。治疗后,两组的血清IL-6和GLA-3水平均显著下降（P<0.05）,且观察组IL-6和GLA-3水平显著低于对照组（P<0.05）。结论 注射用丹参多酚酸联合阿司匹林治疗急性大动脉粥样硬化型脑梗死可促进患者神经功能恢复,改善患者的生活质量,降低炎性因子水平,且安全性较高,具有一定的临床应用价值。     

注射用丹参多酚酸对缺血性脑卒中患者ICAM-1、胆红素及早期神经功能的影响

目的 观察注射用丹参多酚酸对急性缺血性脑卒中患者细胞间黏附因子-1（ICAM-1）、胆红素及早期神经功能的影响，探讨注射用丹参多酚酸可能的作用机制。方法 回顾性以2020年1月—2020年10月在保定市第一中心医院神经内科住院的急性缺血性脑卒中患者100例为研究对象，根据治疗措施不同分为对照组和试验组，每组各50例。对照组为常规抗栓治疗，试验组在对照组基础上加用注射用丹参多酚酸，每次取0.13 g加入0.9%氯化钠注射液250 mL中稀释，静脉滴注，每天1次。两组均连续治疗14 d。在入院第1天、第14天分别收集患者血清，测定ICAM-1、胆红素水平，并应用美国国立卫生研究院卒中量表（NIHSS）评估患者的神经功能，评定两组治疗疗效，并观察治疗期间不良反应发生情况。结果 两组治疗前ICAM-1、胆红素水平及NIHSS评分比较，差异无统计学意义（P＞0.05）。两组治疗后NIHSS评分均较本组治疗前显著降低（P＜0.05），且试验组NIHSS评分明显低于对照组（P＜0.05）。治疗后，对照组胆红素水平较本组治疗前显著降低（P＜0.05），但试验组胆红素水平较本组治疗前显著升高，且高于对照组治疗后水平（P＜0.05）；两组ICAM-1水平均较本组治疗前显著降低（P＜0.05），且试验组ICAM-1水平下降程度较对照组显著（P＜0.05）。试验组的治疗总有效率高于对照组（P＜0.05）。结论 注射用丹参多酚酸可能通过降低ICAM-1水平，升高胆红素水平发挥神经保护作用，改善缺血性脑卒中患者神经功能。     

注射用丹参多酚酸联合阿司匹林对急性脑梗死患者神经功能及血清MMP-7和超敏C反应蛋白的影响

目的 探讨注射用丹参多酚酸联合阿司匹林对急性脑梗死患者神经功能及血清基质金属蛋白酶-7（MMP-7）和超敏C反应蛋白（hs-CRP）的影响。方法 选取2017年8月-2018年10月保定市第一中心医院收治的急性脑梗死患者100例为研究对象,采用随机数字表法将患者分为对照组（49例）和观察组（50例）。对照组给予阿司匹林肠溶片,100 mg/次,晨起空腹温水服用,1次/d。观察组在对照组的基础上静脉滴注丹参多酚酸,0.13 g加入0.9%的氯化钠溶液250 mL。两组均持续治疗14 d。比较两组患者治疗前后的美国国立卫生研究院卒中量表（NIHSS）评分、基质金属蛋白酶-7（MMP-7）及超敏C反应蛋白（hs-CRP）水平。结果 治疗后,两组NIHSS评分均明显降低,同组治疗前后比较差异具有统计学意义（P<0.05）;且观察组NIHSS评分显著低于对照组（P<0.05）。治疗后,两组患者血清MMP-7和hs-CRP水平均显著降低,同组治疗前后比较差异具有统计学意义（P<0.05）;且观察组MMP-7和hs-CRP水平显著低于对照组（P<0.05）。结论 在常规脑梗死治疗基础加用注射用丹参多酚酸应用于急性脑梗死患者,可有效降低其血清MMP-7和hs-CRP水平,显著提高脑梗死患者的NIHSS评分,且安全性好,具有一定的临床推广应用价值。     

消栓通络胶囊联合尤瑞克林治疗急性脑梗死的临床研究

目的 观察消栓通络胶囊联合尤瑞克林治疗急性脑梗死的临床疗效。方法 选择2019年5月—2022年5月在石家庄市人民医院诊治的106例急性脑梗死患者,按照随机数字表法分对照组（53例）和治疗组（53例）。对照组静脉滴注注射用尤瑞克林,0.15PNA单位/次,溶于生理盐水100mL,1次/d。在对照组的基础上,治疗组口服消栓通络胶囊,6粒/次,3次/d。两组用药14d。观察两组患者临床疗效,比较治疗前后两组患者症状改善时间,NIHSS评分,Barthel指数,血清细胞间黏附分子-1（ICAM-1）、血管细胞间黏附分子-1（VCAM-1）、白细胞介素-8（IL-8）和血管内皮生长因子（VEGF）水平,及不良反应。结果 治疗后,治疗组总有效率（98.11%）明显高于对照组（81.13%,P＜0.05）。治疗后,治疗组症状改善时间均明显早于对照组（P＜0.05）。治疗后,两组NIHSS评分明显降低,而Barthel指数评分明显升高（P＜0.05）,且治疗组评分明显好于对照组（P＜0.05）。治疗后,两组血清IL-8、ICAM-1、VCAM-1水平明显降低,而VEGF水平明显升高（P＜0.05）,且治疗组血清因子水平明显好于对照组（P＜0.05）。治疗后,治疗组患者不良反应发生率明显低于对照组（P＜0.05）。结论 消栓通络胶囊联合注射用尤瑞克林治疗急性脑梗死效果确切,可有效改善患者缺血区域血供,改善脑神经功能。     

注射用丹参多酚酸治疗脑梗死急性期疗效及对Hcy、D-二聚体和hs-CRP水平的影响

目的 探讨注射用丹参多酚酸治疗脑梗死急性期患者的疗效及对同型半胱氨酸（Hcy）、D-二聚体和超敏C反应蛋白（hs-CRP）水平影响。方法 选择2016年1月—2019年1月于安阳市第六人民医院收治的脑梗死急性期患者102例,随机分为对照组51例与治疗组51例。对照组患者常规治疗,治疗组在对照组基础上联用注射用丹参多酚酸（100 mg+250 mL的0.9%氯化钠溶液中,静脉滴注,1次/d）。两组疗程均为2周,比较两组疗效,治疗前后日常生活活动能力指数（Balthel指数）评分、蒙特利尔认知评估量表（MoCA）评分和神经功能缺损程度评分（NIHSS评分）变化,血清Hcy、D-二聚体和hs-CRP水平变化及不良反应。结果 治疗组治疗总有效率（92.16%）高于对照组（70.59%）（P<0.05）。治疗后,两组Balthel指数评分和MoCA评分较治疗前升高,而NIHSS评分较治疗前降低（P<0.05）;治疗组Balthel指数评分和MoCA评分高于对照组,而NIHSS评分低于对照组（P<0.05）。治疗后,两组血清Hcy、D-二聚体和hs-CRP水平较治疗前降低（P<0.05）;且治疗组血清Hcy、D-二聚体和hs-CRP水平低于对照组（P<0.05）。结论 注射用丹参多酚酸治疗脑梗死急性期患者疗效良好,可降低Hcy、D-二聚体和hs-CRP水平,值得临床借鉴。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.